ArticleScientific reports2020
Comparative analysis of pathophysiological parameters between emphysematous smokers and emphysematous patients with COPD.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- PHLDA1 knockdown exacerbates emphysema in COPD by attenuating proliferation of alveolar type II cells via modulating GLI1 nuclear translocation.Cellular and molecular life sciences : CMLS · 2026Article
- Advanced models for respiratory disease and drug studies.Medicinal research reviews · 2023Review
- A Macrophage-Related Gene Signature for Identifying COPD Based on Bioinformatics and ex vivo Experiments.Journal of inflammation research · 2023Article
- Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD.Journal of inflammation (London, England) · 2022Review
- Screening and identification of tissue-infiltrating immune cells and genes for patients with emphysema phenotype of COPD.Frontiers in immunology · 2022Article
- The Role of ABC Transporters in Lipid Metabolism and the Comorbid Course of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2021Review
- Identification of Proteomic Signatures in Chronic Obstructive Pulmonary Disease Emphysematous Phenotype.Frontiers in molecular biosciences · 2021Article
- Oxidative stress mediates the apoptosis and epigenetic modification of the Bcl-2 promoter via DNMT1 in a cigarette smoke-induced emphysema model.Respiratory research · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emphysematous smokers with normal spirometry form a considerable proportion of the clinical population. However, despite presenting with respiratory symptoms and activity limitation, they cannot be diagnosed with chronic obstructive lung disease (COPD) according to current criteria. Thus, we aimed to determine whether emphysema in smokers has a different pathogenesis from that in patients with COPD. We compared 12 pairs of lung tissue samples from emphysematous patients with normal spirometry and COPD, and determined the degree of emphysema using computed tomography. With a focus on COPD-related pathogenesis, we independently assessed inflammatory response, protease-antiprotease balance, oxidative stress, and apoptosis in both groups. Both groups showed similar pathological changes at a comparable degree of emphysema; the expression of inflammatory factors was comparable, with overexpression of proteases and decreased levels of antiproteases. Moreover, there was no significant difference in the activities of glutathione and superoxide dismutase, and expression of apoptosis-related factors. In conclusion, emphysema in smokers with normal spirometry and in patients with COPD had similar pathogenesis. Forced expiratory volume in 1 second cannot be used as the sole diagnostic criterion in patients with COPD; early intervention is of great importance to such patients.
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